Current treatments for depression and PTSD only suppress symptoms, if they work at all. What if we could prevent these diseases from developing altogether? Neuroscientist and TED Fellow Rebecca Brachman shares the story of her team’s accidental discovery of a new class of drug that, for the first time ever, could prevent the negative effects of stress — and boost a person’s ability to recover and grow. Learn how these resilience-enhancing drugs could change the way we treat mental illness.
This talk was presented at an official TED conference, and was featured by our editors on the home page.
via Rebecca Brachman: A new class of drug that could prevent depression and PTSD | TED Talk
- Using a drug already approved for clinical trials, researchers were able to reduce brain damage and boost the growth of new brain cells in mice suffering from strokes.
- The research offers new hope to those dealing with the aftermath of strokes, which are the fifth leading cause of death in the United States.
OLD DRUG, NEW TREATMENT
Researchers from the University of Manchester have developed a new treatment that could limit the damage caused by strokes and also promote repair in the affected area of the brain. What’s more, the drug they’re using has already been clinically approved.
The researchers’ study is published in Brain, Behavior and Immunity, and it recounts how they developed their treatment using mice bred to develop ischemic strokes, the most prevalent type of stroke and one that occurs when an artery that supplies oxygen-rich blood to the brain is blocked. Soon after the mice experienced a stroke, the researchers treated them with interleukin-1 receptor antagonist (IL-1Ra), an anti-inflammatory drug that is already licensed for use in treating rheumatoid arthritis.
They noticed a reduction in the amount of brain damage typically observed after a stroke and also noted that the drug boosted neurogenesis (the birth of new cells) in the areas that did experience brain damage in the days following the treatment. The mice even regained the motor skills they lost due to the stroke.
HOPE FOR A CURE
Stroke is the fifth leading cause of death in the United States and about 800,000 people suffer from one each year, according to the Centers for Disease Control and Prevention (CDC). They occur when the flow of blood to the brain is interrupted, usually due to a blood clot or a buildup of fat that broke off from the arteries and traveled to the brain. The condition is extremely dangerous because brain cells can die within a few minutes of the stroke, causing permanent damage or even death.
We still don’t have a treatment to adequately prevent or reverse the damage to the brain caused by strokes, but the Manchester researchers believe that their development could change that. Though they are still in early stages of clinical trials, they hope to eventually move on to larger trials and eventually human testing. Together with other research, this new study offers hope to the thousands of people whose lives are impacted by strokes worldwide.
Source: This FDA Approved Drug Could Permanently Repair Brain Damage in Stroke Victims
There is currently no therapeutic drug treatment for traumatic brain injury (TBI) despite decades of experimental clinical trials. This may be because the mechanistic pathways for improving TBI outcomes have yet to be identified and exploited. As such, there remains a need to seek out new molecular targets and their drug candidates to find new treatments for TBI. This review presents supporting evidence for cathepsin B, a cysteine protease, as a potentially important drug target for TBI. Cathepsin B expression is greatly up-regulated in TBI animal models, as well as in trauma patients. Importantly, knockout of the cathepsin B gene in TBI mice results in substantial improvements of TBI-caused deficits in behavior, pathology, and biomarkers, as well as improvements in related injury models. During the process of TBI-induced injury, cathepsin B likely escapes the lysosome, its normal subcellular location, into the cytoplasm or extracellular matrix (ECM) where the unleashed proteolytic power causes destruction via necrotic, apoptotic, autophagic, and activated glia-induced cell death, together with ECM breakdown and inflammation. Significantly, chemical inhibitors of cathepsin B are effective for improving deficits in TBI and related injuries including ischemia, cerebral bleeding, cerebral aneurysm, edema, pain, infection, rheumatoid arthritis, epilepsy, Huntington’s disease, multiple sclerosis, and Alzheimer’s disease. The inhibitor E64d is unique among cathepsin B inhibitors in being the only compound to have demonstrated oral efficacy in a TBI model and prior safe use in man and as such it is an excellent tool compound for preclinical testing and clinical compound development. These data support the conclusion that drug development of cathepsin B inhibitors for TBI treatment should be accelerated.
Source: Frontiers | Cathepsin B is a New Drug Target for Traumatic Brain Injury Therapeutics: Evidence for E64d as a Promising Lead Drug Candidate | Neurotrauma